Browsing by Author "Aleksic, Nikola (36105795700)"

Background: Angiofollicular lymphoid hyperplasia (Castleman's disease) is a rare inflammatory condition. Its cause is unknown and it can be both localized and general. Eighty-six percent of lesions are found in the mediastinum or hilum, and 91% are of the hyaline vascular type. Although Castleman's disease is primarily involving the chest and retroperitoneum, it may also involve neck and axilla in 2-4% of cases. In this article, we present a very rare case of Castleman's disease causing axillary artery pseudoaneurysm. Methods and Results: A 30-year-old woman patient presented with pulsating tumefaction of the left arm which was 3.5 × 10 cm in size, and became evident 15 days before admission. History revealed that she suffered trauma of the left upper arm in childhood; therefore, it was suspected that tumefaction may be due to a post-traumatic aneurysm. Duplex scan and multislice computed tomography examinations were performed and an axillary artery pseudoaneurysm was diagnosed. Since intraoperatively the tumefaction resembled the tumorous formation but not the aneurysmal wall, specimens were sent for pathohistological analysis. Arterial reconstruction was performed using autologous vein graft. Pathohistological findings showed vascular type of angiofollicular lymphoid hyperplasia. Conclusion: Although angiofollicular lymphoid hyperplasia is rarely localized in the axillary area, this disease should also be considered when axillary artery pseudoaneurysm is diagnosed. © 2010 Annals of Vascular Surgery Inc.

Purpose: Carotid artery stenting (CAS) is an option for carotid restenosis (CR) treatment with favorable outcomes. However, CAS has also emerged as an alternative to carotid endarterectomy (CEA) for the management of patients with primary carotid stenosis. This study aimed to report CR rates after CAS was performed in patients with primary lesions versus restenosis after CEA, to identify predictors of CR, and to report both neurological and overall outcomes. Materials and methods: From January 2000 to September 2018, a total of 782 patients were divided into 2 groups: The CAS (prim) group consisted of 440 patients in whom CAS was performed for primary lesions, and the CAS (res) group consisted of 342 patients with CAS due to restenosis after CEA. Indications for CAS were symptomatic stenosis/restenosis >70% and asymptomatic stenosis/restenosis >85%. A color duplex scan (CDS) of carotid arteries was performed 6 months after CAS, after 1 year, and annually afterward. Follow-up ranged from 12 to 88 months, with a mean follow-up of 34.6±18.0 months. Results: There were no differences in terms of CR rate between the patients in the CAS (prim) and CAS (res) groups (8.7% vs 7.2%, χ2=0.691, p=0.406). The overall CR rate was 7.9%, whereas significant CR (>70%) rate needing re-intervention was 5.6%, but there was no difference between patients in the CAS (prim) and CAS (res) groups (6.4% vs 4.7%, p=0.351). Six independent predictors for CR were smoking, associated previous myocardial infarction and angina pectoris, plaque morphology, spasm after CAS, the use of FilterWire or Spider Fx cerebral protection devices, and time after stenting. A carotid restenosis risk index (CRRI) was created based on these predictors and ranged from –7 (minimal risk) to +10 (maximum risk); patients with a score >–4 were at increased risk for CR. There were no differences in terms of neurological and overall morbidity and mortality between the 2 groups. Conclusions: There was no difference in CR rate after CAS between the patients with primary stenosis and restenosis after CEA. A CRRI score >–4 is a criterion for identifying high-risk patients for post-CAS CR that should be tested in future randomized trials. © The Author(s) 2022.

Background: Inflammation is one of the mechanisms that leads to carotid restenosis (CR). The aim of this study was to examine the influence of increased values of inflammation markers (high-sensitivity C-reactive protein [hs-CRP], C3 complement, and fibrinogen) on CR development after eversion carotid endarterectomy (CEA). Methods: A consecutive 300 patients were included in the study, in which eversion CEA was performed between March 1 and August 1, 2010. Demographic data, atherosclerosis risk factors, comorbidities, and ultrasound plaque characteristics were listed in relation to potential risk factors for CR. Serum concentrations of hs-CRP, fibrinogen, and C3 complement were taken just before surgery (6 hours); 48 hours after CEA; and during regular checkups at 1 month, 6 months, 1 year, and 2 years. An “inflammatory score” was also created, which consisted of six predictive values of inflammatory markers (hs-CRP just before and just after CEA, fibrinogen just before and just after CEA, and C3 complement just before and just after CEA) with a maximum score of 6 and a minimum score of 0. At every follow-up visit to the outpatient clinic, ultrasound assessment of the carotid artery for restenosis was done. Results: Our results showed an increased risk of early CR within 1 year in patients with increased hs-CRP before CEA (6 hours) and increased fibrinogen 48 hours after surgery and in patients not taking aspirin after CEA. Sex was determined to be an independent predictor of CR, with female patients having a higher risk (P =.002). Male patients taking aspirin with an inflammatory score >2 had an increased risk for restenosis compared with male patients with inflammatory score <2. Not taking aspirin after CEA and fibrinogen (48 hours) were the strongest predictors, and the Fisher equation incorporating these predictors was used to predict CR. A computer program was created to calculate whether the patient was at high or low risk for CR by selecting whether the patient was taking aspirin (yes or no) and whether fibrinogen was increased 48 hours after CEA (yes or no) and to display the recommended therapeutic algorithm consisting of aspirin, clopidogrel, cilostazol, and statins. Conclusions: Increased hs-CRP before CEA, increased fibrinogen 48 hours after CEA, and not taking aspirin were the main predictors of early CR. With the clinical implementation of the Fisher equation, it is possible to identify patients at high risk for early CR and to apply an aggressive therapeutic algorithm, finally leading to a decreased CR rate. © 2017 Society for Vascular Surgery